ROLES OF FRUCTOSE IN METABOLIC-DYSFUNCTION ASSOCIATED FATTY LIVER DISEASE AND RENAL DYSFUNCTION IN ALBINO MOUSE
Abstract
ABSTRACT
Metabolic-dysfunction Associated Fatty Liver Disease (MAFLD) previously referred to as Nonalcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease through changes in lifestyle and dietary habits involving diets high in fats and carbohydrates. NAFLD is characterized by excessive accumulation of fat and steatosis, which progresses to non-alcoholic steatohepatitis (NASH), liver fibrosis and cirrhosis. Fructose induced – steatosis are also strongly associated with and kidney injury. The present study was designed to investigate the roles of fructose in metabolic-dysfunction associated fatty liver disease and renal dysfunction in albino mouse. Eighteen (18) male albino mice (17–32 g) were randomly assigned into three treatment groups; 6 in group I (the control group), 6 in group II (the 20% fructose group) and 6 in group III (the 30% fructose group). All treatments lasted for a period of 21 days. Fructose induced a significant weight gain in the groups administered with fructose relative to the control group. Total cholesterol and Triglyceride level increased in the plasma and significantly (p < 0.05) in the liver of fructose-treated mice relative to the control group. There was also a significant increases (p < 0.05) in the oxidative stress biomarker (malondialdehyde, MDA) level followed by a significant decrease in levels/activities of hepatic and renal antioxidants (Reduced Glutathione (GSH), Glutathione peroxidase (GPx), Superoxide Dismutase (SOD) and Catalase, CAT). additionally, the level of nitric oxide (NO) increased in liver and kidney homogenate relative to the control, followed by increase in plasma hepatic biomarkers (activities of alanine aminotransferase, ALT and aspartate aminotransferase, AST) and renal function biomarkers (Urea and creatinine). Overall, data from this study indicated a significant weight gain, elevated hepatic triglycerides, oxidative stress and hepatocellular injury which are contributors to the development of fatty liver disease. Elevated renal function biomarkers suggests potential renal dysfunction related to fructose administration in albino mouse. Further studies with longer duration of fructose treatment is recommended to further understand the mechanism of fructose – induced fatty liver disease in albino mouse
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